AustralieFrV1, PascalFrancis, Curation, bibRecord, 005C93

Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Identifieur interne : 005C93 ( PascalFrancis/Curation ); précédent : 005C92; suivant : 005C94

Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Auteurs : Bruno Verges [France] ; Martin Adiels [Suède] ; Jan Boren [Suède] ; Peter Hugh Barrett [Australie] ; Gerald F. Watts [Australie] ; Dick Chan [Australie] ; Laurence Duvillard [France] ; Sanni Söderlund [Finlande] ; Niina Matikainen [Finlande] ; Juhani Kahri [Finlande] ; Isabelle Robin [France] ; Marja-Riitta Taskinen [Finlande]

Source :

The Journal of clinical endocrinology and metabolism [ 0021-972X ] ; 2014.

RBID : Pascal:15-0000333

Descripteurs français

Pascal (Inist)
- Obésité viscérale, Cinétique, Lipoprotéine VLDL, Lipoprotéine HDL, Catabolisme, Etude multicentrique, Traceur, Endocrinologie, Maladie métabolique, Nutrition.
Wicri :
- topic : Nutrition.

English descriptors

KwdEn :
- Catabolism, Endocrinology, Kinetics, Lipoprotein HDL, Lipoprotein VLDL, Metabolic diseases, Multicenter study, Nutrition, Tracers, Visceral obesity.

Abstract

Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL, VLDL₂) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-l fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity. Results: In a multivariate analysis, among the morphological and biological parameters that may predict apoA-1 FCR, liver fat (β = .400, P = .003), and VLDL₁-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL₁-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL,-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed. Conclusions: We show that VLDL, is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL₁-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL₁-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL₁ metabolism is an important modulator of HDL apoA-I catabolism.

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A11	`03`	`1`		`@1 BOREN (Jan)`
A11	`04`	`1`		`@1 BARRETT (Peter Hugh)`
A11	`05`	`1`		`@1 WATTS (Gerald F.)`
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A11	`07`	`1`		`@1 DUVILLARD (Laurence)`
A11	`08`	`1`		`@1 SÖDERLUND (Sanni)`
A11	`09`	`1`		`@1 MATIKAINEN (Niina)`
A11	`10`	`1`		`@1 KAHRI (Juhani)`
A11	`11`	`1`		`@1 ROBIN (Isabelle)`
A11	`12`	`1`		`@1 TASKINEN (Marja-Riitta)`
A14	`01`			`@1 Department of Endocrinology-Diabetology, University Hospital @2 21000 Dijon @3 FRA @Z 1 aut. @Z 11 aut.`
A14	`02`			`@1 Department of Medical Biology, University Hospital @2 21000 Dijon @3 FRA @Z 7 aut.`
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A14	`04`			`@1 Department of Molecular and Clinical Medicine University of Gothenburg @2 405 30 Gothenburg @3 SWE @Z 2 aut. @Z 3 aut.`
A14	`05`			`@1 Department of Mathematical Sciences, University of Gothenburg @2 405 30 Gothenburg @3 SWE @Z 2 aut.`
A14	`06`			`@1 Faculty of Engineering, Computing, and Mathematics, University of Western Australia @2 Perth, Western Australia 6872 @3 AUS @Z 4 aut.`
A14	`07`			`@1 Lipid Disorders Clinic, Metabolic Research Centre, Department of Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia @2 Perth, Western Australia 6847 @3 AUS @Z 4 aut. @Z 5 aut. @Z 6 aut.`
A14	`08`			`@1 Heart and Lung Centre, Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, Helsinki University Central Hospital @2 00290 Helsinki @3 FIN @Z 8 aut. @Z 9 aut. @Z 12 aut.`
A14	`09`			`@1 Department of Medicine, Helsinki University Central Hospital @2 00290 Helsinki @3 FIN @Z 9 aut. @Z 10 aut.`
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C01	`01`		`ENG`	@0 Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL, VLDL₂) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-l fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity. Results: In a multivariate analysis, among the morphological and biological parameters that may predict apoA-1 FCR, liver fat (β = .400, P = .003), and VLDL₁-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL₁-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL,-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed. Conclusions: We show that VLDL, is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL₁-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL₁-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL₁ metabolism is an important modulator of HDL apoA-I catabolism.
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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study</title>
<author><name sortKey="Verges, Bruno" sort="Verges, Bruno" uniqKey="Verges B" first="Bruno" last="Verges">Bruno Verges</name>
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<author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name>
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<affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Lipid Disorders Clinic, Metabolic Research Centre, Department of Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia</s1>
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<s3>AUS</s3>
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<author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name>
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<author><name sortKey="Chan, Dick" sort="Chan, Dick" uniqKey="Chan D" first="Dick" last="Chan">Dick Chan</name>
<affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Lipid Disorders Clinic, Metabolic Research Centre, Department of Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia</s1>
<s2>Perth, Western Australia 6847</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<country>Australie</country>
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<author><name sortKey="Duvillard, Laurence" sort="Duvillard, Laurence" uniqKey="Duvillard L" first="Laurence" last="Duvillard">Laurence Duvillard</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Medical Biology, University Hospital</s1>
<s2>21000 Dijon</s2>
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<author><name sortKey="Soderlund, Sanni" sort="Soderlund, Sanni" uniqKey="Soderlund S" first="Sanni" last="Söderlund">Sanni Söderlund</name>
<affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Heart and Lung Centre, Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, Helsinki University Central Hospital</s1>
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<sZ>8 aut.</sZ>
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<affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Heart and Lung Centre, Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, Helsinki University Central Hospital</s1>
<s2>00290 Helsinki</s2>
<s3>FIN</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Department of Medicine, Helsinki University Central Hospital</s1>
<s2>00290 Helsinki</s2>
<s3>FIN</s3>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
</affiliation>
</author>
<author><name sortKey="Kahri, Juhani" sort="Kahri, Juhani" uniqKey="Kahri J" first="Juhani" last="Kahri">Juhani Kahri</name>
<affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Department of Medicine, Helsinki University Central Hospital</s1>
<s2>00290 Helsinki</s2>
<s3>FIN</s3>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
<country>Finlande</country>
</affiliation>
</author>
<author><name sortKey="Robin, Isabelle" sort="Robin, Isabelle" uniqKey="Robin I" first="Isabelle" last="Robin">Isabelle Robin</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Endocrinology-Diabetology, University Hospital</s1>
<s2>21000 Dijon</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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<country>France</country>
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<author><name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
<affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Heart and Lung Centre, Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, Helsinki University Central Hospital</s1>
<s2>00290 Helsinki</s2>
<s3>FIN</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>12 aut.</sZ>
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<country>Finlande</country>
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<series><title level="j" type="main">The Journal of clinical endocrinology and metabolism</title>
<title level="j" type="abbreviated">J. clin. endocrinol. metab.</title>
<idno type="ISSN">0021-972X</idno>
<imprint><date when="2014">2014</date>
</imprint>
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<seriesStmt><title level="j" type="main">The Journal of clinical endocrinology and metabolism</title>
<title level="j" type="abbreviated">J. clin. endocrinol. metab.</title>
<idno type="ISSN">0021-972X</idno>
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</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Catabolism</term>
<term>Endocrinology</term>
<term>Kinetics</term>
<term>Lipoprotein HDL</term>
<term>Lipoprotein VLDL</term>
<term>Metabolic diseases</term>
<term>Multicenter study</term>
<term>Nutrition</term>
<term>Tracers</term>
<term>Visceral obesity</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Obésité viscérale</term>
<term>Cinétique</term>
<term>Lipoprotéine VLDL</term>
<term>Lipoprotéine HDL</term>
<term>Catabolisme</term>
<term>Etude multicentrique</term>
<term>Traceur</term>
<term>Endocrinologie</term>
<term>Maladie métabolique</term>
<term>Nutrition</term>
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<front><div type="abstract" xml:lang="en">Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL, VLDL<sub>2</sub>
) kinetics, liver fat, or visceral adiposity, remain to be investigated. Objectives: Our aim was to study the associations between HDL apolipoprotein (apo)-A-l fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat. Design: We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity. Results: In a multivariate analysis, among the morphological and biological parameters that may predict apoA-1 FCR, liver fat (β = .400, P = .003), and VLDL<sub>1</sub>
-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL<sub>1</sub>
-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL,-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed. Conclusions: We show that VLDL, is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL<sub>1</sub>
-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL<sub>1</sub>
-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL<sub>1</sub>
 metabolism is an important modulator of HDL apoA-I catabolism.</div>
</front>
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<fA14 i1="06"><s1>Faculty of Engineering, Computing, and Mathematics, University of Western Australia</s1>
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<sZ>8 aut.</sZ>
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-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL<sub>1</sub>
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-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL<sub>1</sub>
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Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

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